INTRODUCTION: Advanced magnetic resonance imaging (MRI) techniques provide metabolic/hemodynamic information that is useful in the diagnosis of ischemic stroke. To date, however, their application in intracerebral hemorrhage (ICH) has been limited. We postulate that these MRI techniques may help define mechanisms of secondary damage and assess effects of therapeutic interventions in perihematoma tissue after ICH. METHODS: A 44-year-old woman presented with severe headache resulting from a right temporal ICH. After developing neurological deterioration 5 days after the bleed, the patient underwent evacuation of the hematoma. Specimen pathology suggested the presence of a small vascular malformation. Diffusion- and perfusion-weighted imaging as well as proton magnetic resonance spectroscopic imaging (1H-MRSI) investigations to assess perihematoma brain tissue metabolic and circulatory profiles were performed before and after hematoma evacuation. RESULTS: Pre-operative results showed mild oligemia posterior to the hematoma, increased average diffusion coefficient (DAV), and normal perihematoma N-acetyl-aspartate (NAA) concentration on 1H-MRSI. This profile was interpreted as inconsistent with ischemia (as defined by reduced DAV and NAA) but compatible with perihematoma inflammation (as defined by elevated DAV and lactate signal). Postsurgical MRI investigations showed near normalization of the perfusion deficit. CONCLUSION: We postulate that mass effect produced by the hematoma, and perhaps inflammation, can induce perilesional reduced cerebral perfusion in a reversible manner.
INTRODUCTION: Advanced magnetic resonance imaging (MRI) techniques provide metabolic/hemodynamic information that is useful in the diagnosis of ischemic stroke. To date, however, their application in intracerebral hemorrhage (ICH) has been limited. We postulate that these MRI techniques may help define mechanisms of secondary damage and assess effects of therapeutic interventions in perihematoma tissue after ICH. METHODS: A 44-year-old woman presented with severe headache resulting from a right temporal ICH. After developing neurological deterioration 5 days after the bleed, the patient underwent evacuation of the hematoma. Specimen pathology suggested the presence of a small vascular malformation. Diffusion- and perfusion-weighted imaging as well as proton magnetic resonance spectroscopic imaging (1H-MRSI) investigations to assess perihematoma brain tissue metabolic and circulatory profiles were performed before and after hematoma evacuation. RESULTS: Pre-operative results showed mild oligemia posterior to the hematoma, increased average diffusion coefficient (DAV), and normal perihematoma N-acetyl-aspartate (NAA) concentration on 1H-MRSI. This profile was interpreted as inconsistent with ischemia (as defined by reduced DAV and NAA) but compatible with perihematoma inflammation (as defined by elevated DAV and lactate signal). Postsurgical MRI investigations showed near normalization of the perfusion deficit. CONCLUSION: We postulate that mass effect produced by the hematoma, and perhaps inflammation, can induce perilesional reduced cerebral perfusion in a reversible manner.
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